Endo-Thermal Heat Induced

Thrombosis (E-HIT)

Michael Ombrellino MD FACS

The Cardiovascular Care Group

Clinical Associate Professor of Surgery Rutgers

School of Medicine

E-HIT

• Objectives:

–What is E-HIT?

–How do I report it?

–How do I treat it?

E-HIT• Late 1990’s:

RFA and EVLT were introduced as a minimally invasive

treatment options for axial vein reflux of the GSV and SSV as

an alternative to saphenous stripping and ligation.

– The incompetent saphenous vein is purposely thrombosed (closed) by

means of damaging the intimal portion of the vein wall by a heat

generating transducer at the end of a catheter.

– Radiofrequency or laser generated energy induces thermal damage.

Radiofrequency Ablation

E-HIT

• 2004

Higorani et al, JVS vol 40, issue 3 Sept 2004;500-504

Deep Venous Thrombosis after Radiofrequency Ablation of the GSV: A word of

caution

16% incidence of DVT

• 2005-2006:

Kabnick LS, Ombrellino M, Agis H et al

Endovenous heat induced thrombosis (EHIT) at the superficial deep venous junction: a

new post-treatment clinical entity classification and potential treatment strategies

18th annual meeting of American Venous Forum, Miami Fl

EHIT occurs when the clinically induced thrombus extends up to or

beyond the junctions of the deep venous systems

E-HIT

Kabnick Classification Extension of thrombosis:

• Class I: Up to the junction of superficial and deep venous systems.

• Class II: Extends beyond the junction, with a cross-sectional diameter < 50%.

• Class III: Extends beyond the junction, with a cross-sectional diameter > 50%.

• Class IV: Totally occlusive deep venous thrombosis.

Kabnick, Ombrellino et al 2005

E-HIT

E-HIT

• Incidence:

– Overall risk < 1.5-2% (all classes)

• Class I most prevalent

• Class IV extremely rare

• Risk of progressing from class I-II to III-IV is < 3%

• Risk of symptomatic PE progression extremely rare (0.01-0.04%)

• Symptoms:

– 87% asymptomatic

– 10% report groin pain

– 2.9% report leg swelling

Concern that EHIT can lead to DVT/PE which can cause significant disability and rarely death

Santin BJ et al. J Vasc Surg Venous Lymph Disord 2015 Apr;3(2):184-9

Korepta LM et al J Vasc Surg Venous Lymph Disord 2017 May; 5(3):332-8

E-HIT

• Risk Factors:

– Hx of VTE

– CEAP class > 2

– Tobacco use

– Concomitant micro-phlebectomy

• EHIT was significantly higher in patients with concomitant

stab phlebectomies vs RF alone

• 23% vs 7% P=0.01

– Vein diameter > 7.5 mm

– Treatment distance less than 2 – 2.5 cm from junction

Hicks EW et al. J Vasc Surg Venous Lymph Disord 2017 Mar;5(2);200-9

K Kane et al Ann Vasc Surg 2014: 28: 1744-50

E-HIT

Protocol:

• Ultrasound 24-72 hrs post operatively

• Sonographer utilizes B-mode.

• Patient is supine or prone depending on which vein is visualized (SFJ or SPJ).

• Low frequency linear array probe following standard protocol to R/O DVT.

• Deep veins are visualized in cross-sectional plane with compression maneuvers.

E-HIT

If E-HIT is identified and recorded:

• Sonographer changes orientation of probe to visualize the deep veins in the long axis.

• Length of the thrombus into the junction must be measured and cross-sectional diameter calculated.

• It is imperative that the sonographer inform the physician as soon as possible so that potential therapy is not delayed.

E-HIT

IMAGES

E-HIT

• Optimally, post-op scan demonstrates the

induced thrombus to be at least 1-2 cm from

the junction or proximal to the epigastric vein

in the SFJ

E-HIT Class I

E-HIT Class II

Notice the

“Lip” of

thrombus

extending

slightly

across SFJ

E-HIT Class II

E-HIT Class II

E-HIT Class II

E-HIT Class II

E-HIT Class III

E-HIT Class III

E-HIT Class IV

E-HIT

Kabnick Classification Extension of Thrombosis: 2005

Class I: Up to the junction of superficial and deep venous systems. No

treatment

Class II: Extends beyond the junction, with a cross-sectional diameter < 50%.

Low molecular weight heparin until resolution of the thrombus, with ultrasound

follow-up.

Class III: Extends beyond the junction, with a cross-sectional diameter > 50%.

Low molecular weight heparin and vitamin k antagonist for minimum of 3

months.

Class IV: Totally occlusive deep venous thrombosis. Low molecular weight

heparin and vitamin k antagonist minimum of 3 months.

E-HIT

• In 2018 there is no standardized consensus regarding the management and treatment of E-HIT:

– No post-op US and therefore no treatmentSuarez L, Tangney E, O’Donnell TF et al. Cost Analysis and Implication of Routine DVT duplex ultrasound screening after Endovenous ablation. J Vasc Surg Venous Lymphat Disord 2017 Jan; 5 (1): 126-133

• Risk of DVT, PE and death extremely low

• Not cost effective

• Can’t treat what you don’t look for.

E-HIT

– Grade I and II: Daily ASA

– Grade III and IV: AC and repeat US in 1-2 weeks

to track progression or regression. Stop if

regression.

Korepta LM, Watson JJ, Mansour et al. Outcomes of single-center

expirence with classification and treatment of EHIT after endovenous

ablation. J Vasc Surg Venous Lymphat Disord 2017 May; 5 (3): 332-

338

E-HIT

Class I

Watchful waiting,

with serial US

follow-up, 5-7

days. ASA

optional

Class II

Novel oral AC

with serial US

follow up until

thrombus

regression

(< 2weeks)

Class III

At least 4-6 weeks

AC and until US

regression

Class IV

Min 3 months

AC

E-HIT

• Conclusion:– RFA and EVLT should continue to be the preferred and

low risk treatment option

– E-HIT is a low incidence occurrence with proper technique

– E-HIT is rarely symptomatic

– Post op US surveillance is still widely accepted (24-72 hours)

– There are no widely accepted or standardized guidelines for management and treatment of E-HIT

– Once discovered, careful US surveillance is essential

– Immediate communication between the vascular lab and the physician is essential to properly treat the patient